Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Distinct effects of glucose and fructose on gut and liver transcriptome in mice

ABSTRACT: The metabolic syndrome, in which insulin resistance, obesity, atherogenic dyslipidemia and/or hypertension co-occur, is an increasing health problem and can result in various metabolic diseases. A high-sugar consumption, including glucose and fructose, is especially linked to an accelerated development of the metabolic syndrome. Recently the role of the gut has been highlighted in fructose metabolism. Here we studied the effects of a 2-weeks high-fructose diet as compared to a high-dextrose diet and a cornstarch diet, in the small intestine and liver transcriptome of mice. There were no differences in weight gain and food intake between all groups. Liver weight was solely increased in fructose-fed mice. Surprisingly, the glucose-fed mice displayed increased hepatic cholesterol and triglycerides (TGs) content. Overall, we found major effects in the small intestine and only limited changes in the liver transcriptome. The transcriptome of fructose-fed mice was distinct from the dextrose and cornstarch fed mice in both gut and liver, while dextrose and cornstarch feeding only caused differences in the gut transcriptome. Taken together, we underscore the importance of the small intestine in fructose metabolism and this study can provide cues about the harmful effects of dietary fructose and glucose.

ORGANISM(S): Mus musculus

PROVIDER: GSE110710 | GEO | 2025/01/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Deleterious effects of high sucrose diet on intestinal homeostasis in mice

Project description:Objective Western Diet (WD) appears to be an important factor associated with inflammatory bowel diseases (IBD). Refined sugars represent up to 40% of caloric intake in industrialized countries. Unlike fats, the impact of dietary sugar on healthy and inflamed intestine remains poorly described. Design We investigated the effects of a high sucrose diet (HSD) on dextran sulfate sodium (DSS)-induced colitis and on healthy intestine in mice. Several techniques ranging from macroscopic to molecular were used in vivo and direct effect of sugars was examined in cellulo on Caco-2 cell distinguishing differential effect of fructose and glucose. Results During established colitis in mice, HSD aggravated inflammation by increasing gut permeability, raising immune cells in spleen and impairing autophagy process in colonic mucosa. On healthy intestine, HSD caused spontaneous endoscopic lesions, systemic broad immunosuppression and dysregulation of stress-related genes, associated with gut microbiota dysbiosis. Global reprogramming of colonic transcriptome was detected in HSD-fed mice and amazingly, functional annotations demonstrated association with IBD and “colitis” without DSS-treatment. In vitro, low dose of fructose as well as high dose of glucose induced alteration of junctions confirming the deleterious effects of sugar on intestine. These effects seem to be partially reversible on microbiome and transcriptome of mice after switching back to normal diet. Conclusions Our results demonstrated for the first time that under pathological conditions mimicking pre-diabetes (mild hyperglycemia-associated with overweight), a pre-IBD state is established and depending on host sensitivity, in colitis conditions, this exacerbates the inflammation severity by disturbing cell-cell junction organization and autophagy process.

2022-08-21 | GSE151400 | GEO

Intestine epithelial specific hypoxia-inducible factor-1α overexpression on ileum transcriptome

Project description:Background: Intestine epithelial hypoxia-inducible factor-1α (HIF-1α) plays a critical role in maintaining gut barrier function. The aim of this study was to determine genetic activation of intestinal HIF-1α ameliorates western diet-induced metabolic dysfunction–associated steatotic liver disease (MASLD). Methods: Male and/or female intestinal epithelial-specific Hif1α overexpression mice (Hif1α LSL/LSL;VilERcre) and wild-type littermates (Hif1α LSL/LSL) were fed with regular chow diet, high fructose (HFr) or high-fat (60% Kcal) high-fructose diet (HFHFr) for 8 weeks. Metabolic phenotypes were profiled. Results: Male Hif1α LSL/LSL;VilERcre mice exhibited markedly improved glucose tolerance compared to Hif1α LSL/LSL mice in response to HFr diet. Eight weeks HFHFr feeding led to obesity in both Hif1α LSL/LSL;VilERcre and Hif1α LSL/LSL mice. However, male Hif1α LSL/LSL;VilERcre mice exhibited markedly attenuated hepatic steatosis along with reduced liver size and liver weight compared to male Hif1α LSL/LSL mice. Moreover, HFHFr-induced systemic inflammatory responses were mitigated in male Hif1α LSL/LSL;VilERcre mice compared to male Hif1α LSL/LSL mice and those responses were not evident in female mice. Ileum RNA-seq analysis revealed that glycolysis/gluconeogenesis was up in male Hif1α LSL/LSL;VilERcre mice accompanied by increased epithelial cell proliferation. Conclusion: Our data provide evidence that genetic activation of intestinal HIF-1α markedly ameliorates western diet-induced MASLD in a sex-dependent manner. The underlying mechanism is likely attributed to HIF-1α activation induced upregulation of glycolysis, which, in turn, leading to enhanced epithelial cell proliferation and augmented gut barrier function.

2024-10-26 | GSE280362 | GEO

Effect of six different diets on liver gene expression

Project description:Male and female mice (Bl6/J) were fed a chow diet (control 1 and control 2) or a High fat diet (HFD) or a Choline deficient High fat diet (CD HFD) or a Western Diet (WD) or a Western Diet supplemented with glucose and fructose in drinking water (WD glucose fructose) for 15 weeks.

2022-10-31 | GSE159090 | GEO

Transcriptional profiles of intestinal antigen presenting cells from control, HFD-induced prediabetic and diabetic mice

Project description:To determine whether diet-induced changes in gut microbiota modified intestinal immune cell gene expression, we analyzed the transcriptome of antigen presenting cells isolated from the lamina propria of the small intestine of mice fed with different diet.

2015-11-18 | GSE52557 | GEO

Gene expression altered by high-fructose diet feeding and Chrebp deficiency

Project description:Epidemiologic and animal studies implicate overconsumption of fructose in the development of non-alcoholic fatty liver disease, but the molecular mechanisms underlying fructose-induced chronic liver diseases remains largely unknown. We present evidence supporting the essential function of the lipogenic transcription factor ChREBP in mediating adaptation response to fructose and protecting against fructose-induced hepatotoxicity. High-fructose diet (HFrD) activates hepatic lipogenesis via a ChREBP-dependent manner in wildtype mice, while inducing steatohepatitis in Chrebp-KO mice. In Chrebp-KO mouse livers, HFrD reduces levels of molecular chaperones and activates the CHOP-dependent unfolded protein response, whereas administration of chemical chaperone or Chop shRNA rescues liver injury. Gene expression profiling revealed elevated expression of cholesterol biosynthesis genes in Chrebp-KO livers after HFrD, in parallel with increased abundance of nuclear SREBP2. genes expression were compared between livers of wildtype mice fed 70%-fructose-diet v.s. regular chow, and between livers of Chrebp-/- mice v.s. wildtype mice fed 70%-fructose-diet.

2017-03-21 | GSE96820 | GEO

Transcriptional profiles of intestinal CD4 T-cells from control, HFD-induced prediabetic and diabetic mice

Project description:To determine whether diet-induced changes in gut microbiota modified intestinal immune cell gene expression, we analyzed the transcriptome of CD4 T lymphocytes isolated from the lamina propria of the small intestine from mice fed with different diets.

2015-11-18 | GSE52558 | GEO

RNA-sequencing analysis of liver tissue from mice subjected to high-fructose or normal diets during pregnancy.

Project description:During pregnancy, a high-fructose diet (HFrD) exacerbates gestational insulin resistance and is associated with an increased risk of gestational diabetes. The relationship between liver ChREBP and gestational insulin resistance remains elusive. To address this question, we fed pregnant mice either a high-fructose diet or a normal diet. On the 17th day of pregnancy, we extracted liver tissue from the mice and conducted comparative transcriptomic analysis to elucidate the alterations in liver ChREBP during gestational insulin resistance.

2024-02-18 | GSE247892 | GEO

The miR-22-5p/Clec4e axis has diagnostic potential in fructose-induced nonalcoholic fatty liver disease

Project description:Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease.MicroRNAs play roles in the onset and progression of the disease. This study aimed to screen microRNA profiles and potential RNA networks for the diagnosis and treatment of NAFLD. Mice were high-fructose diet (HFrD) fed to induce NAFLD. MicroRNA expression profiles of the livers in HFrD mice and chow-diet fed mice were analyzed by RNA-seq. We successfully constructed high fructose induced NAFLD. There are 13 differentially expressed (DE) miRNAs in the livers of NAFLD mice. In summary, this study furthered our understanding of the genome mechanisms and the development of potential biomarkers for the treatment of fructose-induced NAFLD.

2024-11-15 | GSE263701 | GEO

Transcriptomic analysis of primary hepatocytes and total livers from WT mice fed with CSAA or CDAA-HSHC diet during 2 weeks.

Project description:Mouse primary hepatocytes (PH) and total livers (TL) prepared from C57Bl6 male adult mice which were fed either a CDAA supplemented cholesterol with glucose and fructose or a CSAA diet during 2 weeks.

2024-04-01 | GSE212617 | GEO

Effect ofhepatocyte-specific Chrebp knockout on model of high-fructose diet during pregnancy

Project description:During pregnancy, a high-fructose diet (HFrD) exacerbates gestational insulin resistance and is associated with an increased risk of gestational diabetes. The relationship between liver ChREBP and gestational insulin resistance remains unknown. To address this question, we fed pregnant hChrebp-KO mice and wild-type mice a high-fructose diet, and on the 17th day of pregnancy, we extracted liver tissue from the mice and conducted comparative transcriptomic analysis to elucidate the role of liver ChREBP in gestational insulin resistance."

2024-02-18 | GSE248051 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data